Rictor, short for Rapamycin-insensitive companion of mammalian target of rapamycin, is a key component of the mTORC2 complex. mTORC2 is involved in multiple cellular processes, such as cell survival, migration, and metabolism. It is part of the phosphatidylinositol 3-kinases (PI3K) pathway, and its activation is crucial for the phosphorylation of Akt/PKB at Ser473, which is important for the regulation of various downstream signaling cascades related to cancer and diabetes [2].

In melanoma, low RICTOR levels in BRAF-mutated tumors correlate with a worse clinical outcome. RICTOR-deficient BRAFV600E cells are tolerant to BRAF/MEK inhibitors and show enhanced mitochondrial respiration and NAMPT expression [1].

In renal allograft, Rictor/mTORC2 signaling contributes to interstitial fibrosis by regulating BNIP3-mediated mitophagy. Rictor knockout in endothelial cells alleviates renal vascular endothelial-to-mesenchymal transition and allograft interstitial fibrosis [3].

In lung cancer, amplification of the RICTOR gene and overexpression of Rictor protein can promote cell survival and migration, serving as a potential druggable target [4].

In hepatocellular carcinoma, Rictor binds to wild-type p53 and blocks its activity, playing an oncogenic role. The dynamic nucleocytoplasmic distribution of Rictor is observed during malignant transformation [5].

In conclusion, Rictor, as an essential part of mTORC2, plays a significant role in various biological processes and disease conditions. Gene knockout models in mice have revealed its role in melanoma, renal allograft fibrosis, lung cancer, and hepatocellular carcinoma, providing potential therapeutic targets for these diseases.